Abstract
Redox imbalance and oxidative modifications of macromolecules in brain during aging and neurodegenerative diseases
Highlights
Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the two most common age-related neurodegenerative disorders affecting millions of people worldwide
The exact underlying mechanisms contributing to degenerative changes in AD and PD are multifactorial, oxidative stress induced damage to cellular macromolecules is widely considered to play an important and central role in the pathophysiology and progression of AD and PD.[1,2]
The overall rationale of oxidative stress in aging brain is based on the following premise: (a) the brain contains high levels of unsaturated fatty acids which are vulnerable to oxidation; b) the brain consumes high amounts of oxygen; and c) the brain contains high concentrations of transition metals such as iron (Fe2+) that are key catalysts of oxidative-induced damages[3] For scavenging these free radicals, cells have an extensive antioxidant system
Summary
Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the two most common age-related neurodegenerative disorders affecting millions of people worldwide. The exact underlying mechanisms contributing to degenerative changes in AD and PD are multifactorial, oxidative stress induced damage to cellular macromolecules is widely considered to play an important and central role in the pathophysiology and progression of AD and PD.[1,2] The purpose of this article is to highlight the oxidative stressinduced damages to macromolecules in brain during aging and neurodegenerative disorders.
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